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ALS-linked mutant SOD1 induces ER stress- and ASK1-dependent motor neuron death by targeting Derlin-1.
It is demonstrated that ER stress-induced ASK1 activation, which is triggered by the specific interaction of Derlin-1 with SOD1(mut), is crucial for disease progression of familial ALS.
Signaling Pathways from the Endoplasmic Reticulum and Their Roles in Disease
This review will discuss the molecular mechanisms of the UPR and ER stress-induced apoptosis, as well as the possible roles of ER stress in several diseases.
Amyloid beta induces neuronal cell death through ROS-mediated ASK1 activation.
Results indicate that ROS-mediated ASK1 activation is a key mechanism for Abeta-induced neurotoxicity, which plays a central role in Alzheimer's disease.
Survival and apoptosis signals in ER stress: the role of protein kinases
A novel monoclonal antibody reveals a conformational alteration shared by amyotrophic lateral sclerosis‐linked SOD1 mutants
It is necessary to develop molecular mechanism‐based diagnosis and treatment of ALS caused by SOD1 mutations because it remains controversial whether all of them are disease‐causative mutations.
USP14 inhibits ER-associated degradation via interaction with IRE1alpha.
The Cytoplasmic Domain of Alzheimer's Amyloid-β Protein Precursor Causes Sustained Apoptosis Signal-Regulating Kinase 1/c-Jun NH2-Terminal Kinase-Mediated Neurotoxic Signal via Dimerization
- Y. Hashimoto, T. Niikura, I. Nishimoto
- Biology, ChemistryJournal of Pharmacology and Experimental…
- 1 September 2003
Data indicate that dimerization of AβPPCD triggers ASK1/JNK-mediated neuronal cell death, which allows for the achievement of cell death by short-term anti-AβPP antibody treatment.
Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation
The results indicate that ROS-mediated ASK1 activation is a key mechanism for Aβ-induced neurotoxicity, which plays a central role in Alzheimer's disease.
SOD1 as a molecular switch for initiating the homeostatic ER stress response under zinc deficiency.